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TRACHOMA

Trachoma (previously known as Egyptianophthalmia) is a chronic keratoconjunctivitis,primarily affecting the superficial epithelium ofconjunctiva and cornea simultaneously. It ischaracterised by a mixed follicular and papillaryresponse of conjunctival tissue. It is still one of theleading causes of preventable blindness in the world.The word 'trachoma' comes from the Greek word for'rough' which describes the surface appearance ofthe conjunctiva in chronic trachoma.Table 4.2. Summary of ocular infections caused by chlamydiaGenus ChlamydiaSpecies C. trachomatis C. lymphogranulomatis C. psittacosis(TRIC agent) (Humans) (Humans) (Animals)Serotype A, B, Ba, C D to K L1, L2, L3Ocular Hyperendemic Paratrachoma Lymphogranulomadisease trachoma (– neonatal venereumand adult inclusion conjunctivitisconjunctivitis)Transmission Eye to eye Genitals to eye Genitals to eye DISEASES OF THE CONJUNCTIVA 63EtiologyA. Causative organism. Trachoma is caused by aBedsonian organism, the Chlamydia trachomatisbelonging to the Psittacosis-lymphogranulomatrachoma(PLT) group. The organism is epitheliotropicand produces intracytoplasmic inclusion bodiescalled H.P. bodies (Halberstaedter Prowazekebodies). Presently, 11 serotypes of chlamydia, (A, B,Ba, C, D, E, F, G, H, J and K) have been identifiedusing microimmunofluorescence techniques.Serotypes A, B, Ba and C are associated withhyperendemic (blinding) trachoma, while serotypesD-K are associated with paratrachoma (oculogenitalchlamydial disease).B. Predisposing factors. These include age, sex, race,climate, socioeconomic status and environmentalfactors.1. Age. The infection is usually contracted duringinfancy and early childhood. Otherwise, there isno age bar.2. Sex. As far as sex is concerned, there is generalagreement that preponderance exists in thefemales both in number and in severity of disease.3. Race. No race is immune to trachoma, but thedisease is very common in Jews and comparativelyless common among Negroes.4. Climate. Trachoma is more common in areas withdry and dusty weather.5. Socioeconomic status. The disease is morecommon in poor classes owing to unhygienicliving conditions, overcrowding, unsanitaryconditions, abundant fly population, paucity ofwater, lack of materials like separate towels andhandkerchiefs, and lack of education andunderstanding about spread of contagiousdiseases.6. Environmental factors like exposure to dust,smoke, irritants, sunlight etc. increase the risk ofcontracting disease. Therefore, outdoor workersare more affected in comparison to office workers.C. Source of infection. In trachoma endemic zonesthe main source of infection is the conjunctivaldischarge of the affected person. Therefore,superimposed bacterial infections help intransmission of the disease by increasing theconjunctival secretions.D. Modes of infection. Infection may spread fromeye to eye by any of the following modes:1. Direct spread of infection may occur throughcontact by air-borne or water-borne modes.2. Vector transmission of trachoma is commonthrough flies.3. Material transfer plays an important role in thespread of trachoma. Material transfer can occurthrough contaminated fingers of doctors, nursesand contaminated tonometers. Other sources ofmaterial transfer of infection are use of commontowel, handkerchief, bedding and surma-rods.PrevalenceTrachoma is a worldwide disease but it is highlyprevalent in North Africa, Middle East and certainregions of Sourth-East Asia. It is believed to affectsome 500 million people in the world. There are about150 million cases with active trachoma and about 30million having trichiasis, needing lid surgery.Trachoma is responsible for 15-20 percent of theworld's blindness, being second only to cataract.Clinical profile of trachomaIncubation period of trachoma varies from 5-21 days.Onset of disease is usually insidious (subacute),however, rarely it may present in acute form.Clinical course of trachoma is determined by thepresence or absence of secondary infection. In theabsence of such an infection, a pure trachoma is somild and symptomless that the disease is usuallyneglected. But, mostly the picture is complicated bysecondary infection and may start with typicalsymptoms of acute conjunctivitis. In the earlystages it is clinically indistinguishable from thebacterial conjunctivitis and the term 'trachomadubium'(doubtful trachoma) is sometimes used forthis stage.Natural history. In an endemic area natural historyof trachoma is characterized by the development ofacute disease in the first decade of life whichcontinues with slow progression, until the diseasebecomes inactive in the second decade of life. Thesequelae occur at least after 20 years of the disease.Thus, the peak incidence of blinding sequelae is seenin the fourth and fifth decade of life. 64 Comprehensive OPHTHALMOLOGYSymptoms In the absence of secondary infection, symptomsare minimal and include mild foreign bodysensation in the eyes, occasional lacrimation,slight stickiness of the lids and scanty mucoiddischarge. In the presence of secondary infection, typicalsymptoms of acute mucopurulent conjunctivitisdevelop.SignsA. Conjunctival signs1. Congestion of upper tarsal and fornicealconjunctiva.2. Conjunctival follicles. Follicles (Fig. 4.9 andFig.4.10) look like boiled sagograins and arecommonly seen on upper tarsal conjunctiva andfornix; but may also be present in the lowerfornix, plica semilunaris and caruncle. Sometimes,(follicles may be seen on the bulbar conjunctiva(pathognomic of trachoma).follicular conjunctivitis.3. Papillary hyperplasia. Papillae are reddish, flattopped raised areas which give red and velvetyappearance to the tarsal conjunctiva (Fig. 4.11).Each papilla consists of central core of numerousdilated blood vessels surrounded by lymphocytesand covered by hypertrophic epithelium.Fig. 4.10. Trachomatous inflammation follicular (TF)Structure of follicle. Follicles are formed due toscattered aggregation of lymphocytes and othercells in the adenoid layer. Central part of each follicleis made up of mononuclear histiocytes, fewlymphocytes and large multinucleated cells calledLeber cells. The cortical part is made up of a zoneof lymphocytes showing active proliferation. Bloodvessels are present in the most peripheral part. Inlater stages signs of necrosis are also seen. Presenceof Leber cells and signs of necrosis differentiatetrachoma follicles from follicles of other forms ofFig. 4.9. Signs of active traochoma (diagramatic).Fig. 4.11. Trachomatous inflammation intense (TI)4. Conjunctival scarring (Fig. 4.12), which may beirregular, star-shaped or linear. Linear scar presentin the sulcus subtarsalis is called Arlt's line.5. Concretions may be formed due to accumulationof dead epithelial cells and inspissated mucus inthe depressions called glands of Henle. DISEASES OF THE CONJUNCTIVA 65Fig. 4.12. Trachomatous scarring (TS)Fig. 4.13. Trachomatous pannus : (A) progressive,(B) regressive (diagramatic) and (C) clinical photographB. Corneal signs1. Superficial keratitis may be present in the upperpart.2. Herbert follicles refer to typical follicles presentin the limbal area. These are histologically similarto conjunctival follicles.C3. Pannus i.e., infiltration of the cornea associatedwith vascularization is seen in upper part (Fig.4.13). The vessels are superficial and lie betweenepithelium and Bowman's membrane. Later onBowman's membrane is also destroyed. Pannusmay be progressive or regressive. In progressive pannus, infiltration of cornea isahead of vascularization. In regressive pannus (pannus siccus) vesselsextend a short distance beyond the area ofinfiltration.4. Corneal ulcer may sometime develop at theadvancing edge of pannus. Such ulcers are usuallyshallow which may become chronic and indolent.5. Herbert pits are the oval or circular pittedscars, left after healing of Herbert follicles in thelimbal area (Fig. 4.14).6. Corneal opacity may be present in the upperpart. It may even extend down and involve thepupillary area. It is the end result of trachomatouscorneal lesions.Grading of trachomaMcCallan's classificationMcCallan in 1908, divided the clinical course of thetrachoma into following four stages: Stage I (Incipient trachoma or stage of infiltration).It is characterized by hyperaemia of palpebralconjunctiva and immature follicles. Stage II (Established trachoma or stage of floridinfiltration). It is characterized by appearance ofmature follicles, papillae and progressive cornealpannus.Fig. 4.14. Trachomatous Herbert's pits.AB 66 Comprehensive OPHTHALMOLOGY Stage III (Cicatrising trachoma or stage ofscarring). It includes obvious scarring of palpebralconjunctiva. Stage IV (Healed trachoma or stage of sequelae).The disease is quite and cured but sequelae dueto cicatrisation give rise to symptoms.WHO classificationTrachoma has always been an important blindingdisease under consideration of WHO and thus manyattempts have been made to streamline its clinicalprofile. The latest classification suggested by WHOin 1987 (to replace all the previous ones) is as follows(FISTO):1. TF: Trachomatous inflammation-follicular. It isthe stage of active trachoma with predominantlyfollicular inflammation. To diagnose this stage atleast five or more follicles (each 0.5 mm or morein diameter) must be present on the upper tarsalconjunctiva (Fig. 4.10). Further, the deep tarsalvessels should be visible through the folliclesand papillae.2. TI : Trachomatous inflammation intense. Thisstage is diagnosed when pronouncedinflammatory thickening of the upper tarsalconjunctiva obscures more than half of the normaldeep tarsal vessels (Fig. 4.11).3. TS: Trachomatous scarring. This stage isdiagnosed by the presence of scarring in thetarsal conjunctiva. These scars are easily visibleas white, bands or sheets (fibrosis) in the tarsalconjunctiva (Fig. 4.12).4. TT: Trachomatous trichiasis. TT is labelled whenat least one eyelash rubs the eyeball. Evidence ofrecent removal of inturned eyelashes should alsobe graded as trachomatous trichiasis (Fig. 4.15).5. CO: Corneal opacity. This stage is labelled wheneasily visible corneal opacity is present over thepupil. This sign refers to corneal scarring that isso dense that at least part of pupil margin isblurred when seen through the opacity. Thedefinition is intended to detect corneal opacitiesthat cause significant visual impairment (less than6/18).Sequelae of trachoma1. Sequelae in the lids may be trichiasis (Fig. 4.15),entropion, tylosis (thickening of lid margin), ptosis,madarosis and ankyloblepharon.Fig. 4.15. Trachomatous trichiasis (TT).2. Conjunctival sequelae include concretions,pseudocyst, xerosis and symblepharon.3. Corneal sequelae may be corneal opacity, ectasia,corneal xerosis and total corneal pannus (blindingsequelae).4. Other sequelae may be chronic dacryocystitis,and chronic dacryoadenitis.ComplicationsThe only complication of trachoma is corneal ulcerwhich may occur due to rubbing by concretions, ortrichiasis with superimposed bacterial infection.DiagnosisA. The clinical diagnosis of trachoma is made fromits typical signs; at least two sets of signs should bepresent out of the following:1. Conjunctival follicles and papillae2. Pannus progressive or regressive3. Epithelial keratitis near superior limbus4. Signs of cicatrisation or its sequelaeClinical grading of each case should be done asper WHO classfication into TF, TI, TS, TT or CO.B. Laboratory diagnosis. Advanced laboratory testsare employed for research purposes only. Laboratorydiagnosis of trachoma includes :1. Conjunctival cytology. Giemsa stained smearsshowing a predominantly polymorphonuclearreaction with presence of plasma cells and Lebercells is suggestive of trachoma.2. Detection of inclusion bodies in conjunctivalsmear may be possible by Giemsa stain, iodine DISEASES OF THE CONJUNCTIVA 67stain or immunofluorescent staining, specially incases with active trachoma.3. Enzyme-linked immunosorbent assay (ELISA) forchlamydial antigens.4. Polymerase chain reaction (PCR) is also useful.5. Isolation of chlamydia is possible by yolk-sacinoculation method and tissue culture technique.Standard single-passage McCoy cell culturerequires at least 3 days.6. Serotyping of TRIC agents is done by detectingspecific antibodies using microimmunofluorescence(micro-IF) method. Directmonoclonal fluorescent antibody microscopy ofconjunctival smear is rapid and inexpensive.Differential diagnosis1. Trachoma with follicular hypertrophy must bedifferentiated from acute adenoviral follicularconjunctivitis (epidemic keratoconjunctivitis) asfollows : Distribution of follicles in trachoma is mainly onupper palpebral conjunctiva and fornix, while inEKC lower palpebral conjunctiva and fornix ispredominantly involved. Associated signs such as papillae and pannusare characteristic of trachoma. In clinically indistinguishable cases, laboratorydiagnosis of trachoma helps in differentiation.2. Trachoma with predominant papillaryhypertrophy needs to be differentiated from palpebralform of spring catarrh as follows: Papillae are large in size and usually there istypical cobble-stone arrangement in spring catarrh. pH of tears is usually alkaline in spring catarrh,while in trachoma it is acidic, Discharge is ropy in spring catarrh. In trachoma, there may be associated folliclesand pannus. In clinically indistinguishable cases, conjunctivalcytology and other laboratory tests for trachomausually help in diagnosis.ManagementManagement of trachoma should involve curative aswell as control measures.A. Treatment of active trachomaAntibiotics for treatment of active trachoma may begiven locally or systemically, but topical treatment ispreferred because: It is cheaper, There is no risk of systemic side-effects, and Local antibiotics are also effective againstbacterial conjunctivitis which may be associatedwith trachoma.The following topical and systemic therapyregimes have been recommended:1. Topical therapy regimes. It is best for individualcases. It consists of 1 percent tetracycline or 1percent erythromycin eye ointment 4 times a dayfor 6 weeks or 20 percent sulfacetamide eyedrops three times a day along with 1 percenttetracycline eye ointment at bed time for 6 weeks.The continuous treatment for active trachomashould be followed by an intermittent treatmentespecially in endemic or hyperendemic area.2. Systemic therapy regimes. Tetracycline orerythromycin 250 mg orally, four times a day for3-4 weeks or doxycycline 100 mg orally twicedaily for 3-4 weeks or single dose of 1 gmazithromycin has also been reported to be equallyeffective in treating trachoma.3. Combined topical and systemic therapy regime.It is preferred when the ocular infection is severe(TI) or when there is associated genital infection.It includes: (i) 1 per cent tetracycline orerythromycin eye ointment 4 times a day for 6weeks; and (ii) tetracycline or erythromycin 250mg orally 4 times a day for 2 weeks.B. Treatment of trachoma sequelae1. Concretions should be removed with ahypodermic needle.2. Trichiasis may be treated by epilation, electrolysisor cryolysis (see page 348).3. Entropion should be corrected surgically (seepage 349).4. Xerosis should be treated by artificial tears.C. ProphylaxisSince, immunity is very poor and short lived, soreinfections and recurrences are likely to occur.Following prophylactic measures may be helpfulagainst reinfection of trachoma.1. Hygienic measures. These help a great deal indecreasing the transmission of disease, astrachoma is closely associated with personal 68 Comprehensive OPHTHALMOLOGYhygiene and environmental sanitation. Therefore,health education on trachoma should be given topublic. The use of common towel, handkerchief,surma rods etc. should be discouraged. A goodenvironmental sanitation will reduce the flies. Agood water supply would improve washing habits.2. Early treatment of conjunctivitis. Every case ofconjunctivitis should be treated as early aspossible to reduce transmission of disease.3. Blanket antibiotic therapy (intermittenttreatment). WHO has recommended this regimeto be carried out in endemic areas to minimise theintensity and severity of disease. The regime isto apply 1 percent tetracycline eye ointment twicedaily for 5 days in a month for 6 months.D. Prevention of trachoma blindnessSee page 447.

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